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. 2011 Sep 27;2:484. doi: 10.1038/ncomms1495

Figure 3. TORC2 inhibition and/or TORC1 activation bypass the SMP signal.

Figure 3

(a) Quantitative ray 1 phenotype caused by CeLST8 knockdown in the plx-1 mutant background. (b) Transgenic L3–L4 males (ncEx9005) were subjected to either control or CeLST8 RNAi, and then lysed. FLAG∷LET-363 proteins in the lysate were immunoprecipitated, followed by analysis of IP and lysates. (c) Quantitative ray 1 phenotype in animals overexpressing DAF-15 under the lin-32p in the background of plx-1 or smp-1 smp-2 mutants. (d) Quantitative ray 1 phenotypes caused by loss of LKB1 (par-4), STRAD (strd-1), AMPKα (aak-1 & aak-2) or AMPKβ (aakb-1) in the background of plx-1 mutants. (e) Epidermal ray precursor cells visualized with ajm-1∷gfp in a daf-15(RNAi) male at the early L4 stage. Anterior is left, and dorsal is top. Scale bar, 10 μm. (f) Nomarski image of a tail in a daf-15(RNAi) adult male. An arrow indicates ray 1; an arrowhead, ray 2. Anterior is left, and dorsal is top. Scale bar, 10 μm. (g) Quantitative ray 1 phenotype in animals subjected to ray-specific RNAi against plx-1, let-363 and daf-15. For a,c,d,g: for the quantitative evaluation, the ray 1 phenotypes are categorized into either Level 1 (normal), Level 2 (mildly defective), or Level 3 (severely defective), which are represented by white, grey or black segment of each bar, respectively n=148–234 for each genotype.